The mammalian heart has four chambers for receiving and pumping blood to various parts of the body. During normal operation of the heart, oxygen poor blood returning from the body enters the right atrium via the inferior vena cava, superior vena cava, coronary sinus, or the coronary veins. The right atrium fills and eventually contracts to expel the blood through the tricuspid valve and into the right ventricle. The right ventricle fills full of blood and then contracts beginning from the apex of the ventricle to the base of the ventricle and forces blood through the pulmonary valve to the pulmonary arteries and to the lungs. The blood becomes oxygenated at the lungs and then returns from the lungs to the left atrium via the pulmonary veins. The left atrium contracts to expel blood through the mitral valve and into the left ventricle. The left ventricle then fills full of blood and then contracts beginning from the apex of the ventricle to the base of the ventricle and forces blood through the aortic valve, into the aorta, and eventually to the body tissues.
The major blood supply to the heart is derived from the coronary arteries, two arteries that branch off from the aorta just distal from the aortic valve. The right coronary artery provides blood to the right side of the heart, the left coronary artery supplies blood to the left side of the heart including the left ventricle. Coronary artery disease usually affects the left coronary artery reducing the blood flow to the left ventricle. When the blood flow supplying oxygen and nutrients cannot meet the demands of the heart, the heart becomes ischemic and the patient usually suffers from chest pain (angina). When the flow of blood completely stops due to an occlusion of a coronary artery, the heart muscle becomes very ischemic and will die if blood flow is not restored in a few minutes.
A myocardial infarction occurs when the heart muscle cells die. The dead muscle cells are replaced by scar tissue over a period of a few weeks. The scar tissue is not contractile, therefore it does not contribute to the pumping ability of the heart. In addition, scar tissue is somewhat elastic which further reduces the efficiency of the heart because a portion of the force created by the remaining healthy muscle bulges out of the scarred tissue (i.e., ventricular aneurysm) instead of pumping the blood out of the heart.
If the myocardial infarction is fairly large, the scar tissue will form across the width of the heart and is described as a transmural infarct. The scar tissue will be present both at the endocardial side (inside of the heart) and the epicardial side (outside of the heart). Transmural infarcts are typically indicated when a patient has a Q-wave infarct as diagnosed on an electrocardiogram (ECG).
Transmural infarcts can lead to congestive heart failure, a condition where the heart cannot pump enough blood to the body to maintain the supply of oxygen and nutrients to keep up with the demand. Congestive heart failure is generally treated with lots of rest, low salt diet, and medications such as angiotensin converting enzyme (ACE) inhibitors, digitalis, vasodilators, and diuretics. In some myocardial infarcts the infarct is surgically removed (an infarctectomy or an aneurysmectomy) and the healthy heart is sutured together. This treatment is very invasive and has a high morbidity and mortality rate. Ultimately, most patients with congestive heart failure die of the condition or are given a heart transplant.
The scar that forms in the myocardium is primarily composed of collagen. Collagen demonstrates several unique characteristics not found in other tissues. Intermolecular cross-links provide collagen with unique physical properties of high tensile strength and substantial elasticity. The cross-links in collagen are organized such that the three dimensional protein structure of the natural collagen forms into a rope like structure with striations along the rope. When collagen is heated to temperatures above about 60 to 65 degrees centigrade, it is believed that the cross-links rupture and the protein becomes more globular and less rope like. As the collagen becomes more globular, the collagen shrinks along its axial length. The higher the temperature the collagen is heated, the more globular the collagen becomes and the greater the shrinkage. Collagen can shrink to almost about ½ of its original length. The caliber of the collagen fibers also increases as collagen is heated, up to a four fold increase depending on the temperature.
In a previously filed U.S. patent application Ser. No. 08/768,607 (Dec. 18, 1996) Michael D. Laufer disclosed the use of heat to treat infarcted heart tissue, the disclosure of which is hereby incorporated by reference. The heat would shrink the collagen containing tissue and increase the pumping efficiency of the heart by decreasing the area that was not pumping efficiently. In the Laufer application, it is disclosed that the scar tissue is to be heated to certain temperature ranges, however, it does not disclose specific means to control the temperature to the desired range. Additionally, the application did not disclose a specific device heating element configuration to optimize infarct scar heating throughout the scar.
Animal studies also show that heating the scar tissue to shrink the collagen gave very good initial clinical results, however, chronically the body replaced the denatured collagen with normal collagen and the scar tissue dilated such that the acute results were not maintained.
What is needed therefore is a device and method for heating myocardial scar tissue and controlling the temperature of the tissue to a set temperature range and an optimal heating element to throughly heat the infarct scar. What is also needed is a device and method that maintains the improvement in cardiac function chronically.